ArticleDisease models & mechanisms2011
The tumor suppressor gene Trp53 protects the mouse lens against posterior subcapsular cataracts and the BMP receptor Acvr1 acts as a tumor suppressor in the lens.
Article in Disease models & mechanisms, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Insights into Bone Morphogenetic Protein-(BMP-) Signaling in Ocular Lens Biology and Pathology.Cells · 2021Review
- Leukocyte chemotactic receptor Fpr1 protects against aging-related posterior subcapsular cataract formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Association analysis of polymorphisms rs12997 in ACVR1 and rs1043784 in BMP6 genes involved in bone morphogenic protein signaling pathway in primary angle-closure and pseudoexfoliation glaucoma patients of Saudi origin.BMC medical genetics · 2020Article
- ACVR1 Function in Health and Disease.Cells · 2019Review
- Identification of Novel Gata3 Distal Enhancers Active in Mouse Embryonic Lens.Developmental dynamics : an official publication of the American Association of Anatomists · 2018Article
- Lifetime study in mice after acute low-dose ionizing radiation: a multifactorial study with special focus on cataract risk.Radiation and environmental biophysics · 2018Article
- HSF4 regulates lens fiber cell differentiation by activating p53 and its downstream regulators.Cell death & disease · 2017Article
- Signaling and Gene Regulatory Networks in Mammalian Lens Development.Trends in genetics : TIG · 2017Review
- Transforming Growth Factor β Superfamily Signaling in Development of Colorectal Cancer.Gastroenterology · 2017Review
- Article
- Chromatin remodeling enzyme Snf2h regulates embryonic lens differentiation and denucleation.Development (Cambridge, England) · 2016Article
- Concise Review: Patient-Specific Stem Cells to Interrogate Inherited Eye Disease.Stem cells translational medicine · 2016Review
- The cellular and molecular mechanisms of vertebrate lens development.Development (Cambridge, England) · 2014Review
- Aberrant activation of p53 due to loss of MDM2 or MDMX causes early lens dysmorphogenesis.Developmental biology · 2014Article
- Emerging issues in radiogenic cataracts and cardiovascular disease.Journal of radiation research · 2014Review
- A genetic variant in microRNA target site of TGF-β signaling pathway increases the risk of colorectal cancer in a Chinese population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Article
- Regulation of mouse lens maturation and gene expression by Krüppel-like factor 4.Experimental eye research · 2013Article
- p53 E3 ubiquitin protein ligase homolog regulates p53 in vivo in the adult mouse eye lens.Molecular vision · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We previously found that lenses lacking the Acvr1 gene, which encodes a bone morphogenetic protein (BMP) receptor, had abnormal proliferation and cell death in epithelial and cortical fiber cells. We tested whether the tumor suppressor protein p53 (encoded by Trp53) affected this phenotype. Acvr1 conditional knockout (Acvr1(CKO)) mouse fiber cells had increased numbers of nuclei that stained for p53 phosphorylated on serine 15, an indicator of p53 stabilization and activation. Deletion of Trp53 rescued the Acvr1(CKO) cell death phenotype in embryos and reduced Acvr1-dependent apoptosis in postnatal lenses. However, deletion of Trp53 alone increased the number of fiber cells that failed to withdraw from the cell cycle. Trp53(CKO) and Acvr1;Trp53(DCKO) (double conditional knockout), but not Acvr1(CKO), lenses developed abnormal collections of cells at the posterior of the lens that resembled posterior subcapsular cataracts. Cells from human posterior subcapsular cataracts had morphological and molecular characteristics similar to the cells at the posterior of mouse lenses lacking Trp53. In Trp53(CKO) lenses, cells in the posterior plaques did not proliferate but, in Acvr1;Trp53(DCKO) lenses, many cells in the posterior plaques continued to proliferate, eventually forming vascularized tumor-like masses at the posterior of the lens. We conclude that p53 protects the lens against posterior subcapsular cataract formation by suppressing the proliferation of fiber cells and promoting the death of any fiber cells that enter the cell cycle. Acvr1 acts as a tumor suppressor in the lens. Enhancing p53 function in the lens could contribute to the prevention of steroid- and radiation-induced posterior subcapsular cataracts.
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